Mother-to-child transmission of human T-cell lymphotropic virus type I associated with prolonged breast-feeding.

OBJECTIVES: We assessed the risk of transmitting human T-cell lymphotropic virus type I (HTLV-I) through breast-feeding. STUDY DESIGN/METHODS: To assess the risk of mother-to-child transmission of HTLV-I, 212 HTLV-I-seropositive women and 145 HTLV-I-seronegative women were enrolled in a prospective cohort study conducted in Kingston, Jamaica. Their offspring were examined at regular intervals, and HTLV-I serostatus was determined at each visit. RESULTS: Twenty-eight of the 181 children with at least one postnatal visit born to HTLV-I-seropositive women (and none of the children born to HTLV-I-seronegative women) were persistently seropositive and were considered HTLV-I infected (Kaplan-Meier estimated cumulative incidence, 18%; 95% CI, 12%-24%). Among children observed for at least 24 months, 19 (32%) of 60 children breast fed for 12 months or longer were HTLV-I seropositive, compared with only 8 (9%) of 86 children breast-fed for less than 12 months (relative risk, 3.4; 95% CI, 1.7-6.9). Compared with children weaned at younger ages, transmission of HTLV-I was associated with continued breast-feeding of children who were 12 to 18 months of age (relative hazard, 6.4; 95% CI, 2.1-180.2) and older than 18 months (relative hazard, 18.1; 95% CI, 1.4-29.5). Transmission was also associated with higher maternal antibody titer (a possible marker of virus load), prolonged duration of ruptured membranes during childbirth, and lower maternal income. CONCLUSIONS: These results suggest that limiting the duration of breast-feeding to less than 12 months for children born to HTLV-I-seropositive mothers may significantly reduce mother-to-child transmission of HTLV-I.

Mother-to-child transmission of human T-cell lymphotropic virus type I (HTLV-I) in Jamaica: association with antibodies to envelope glycoprotein (gp46) epitopes.

To study mother-to-child transmission of HTLV-I in Jamaica, we screened antenatal patients in Kingston, Jamaica, from 1983 to 1985. Of 2,329 women, 81 (3.5%) were HTLV-I seropositive. Two to three years later, 36 seropositive mothers were recontacted, and blood was drawn from them and their children. All sera were tested for HTLV-I antibodies, and mother's sera were additionally tested for HTLV-I whole-virus antibody titer, syncytium-inhibition neutralizing antibody titer, and titers to six synthetic peptides from the HTLV-I envelope glycoprotein gp46. Seventeen of 74 (23%) [95% confidence interval (CI) 15-34%] children were seropositive. HTLV-I transmission was associated with breast-feeding duration > 6 months [relative risk (RR) 3.2; CI 0.4-22.1], maternal age > 30 years (RR 2.8; CI 1.0-7.8), and higher maternal whole-virus antibody titer (RR 3.3; CI 1.3-8.5). After controlling for higher whole-virus antibody titer, transmission remained associated with higher titer of neutralizing antibody and higher titer of antibody to the peptide sp4a1, corresponding to amino acids 196-209 of the gp46 envelope glycoprotein. We conclude that mother-to-child transmission of HTLV-I in Jamaica is associated with longer duration of breast-feeding, older age, and higher HTLV-I antibody titer, in particular to a certain immunogenic portion of the gp46 envelope glycoprotein.